Medical Biology Research Center, Health Technology Institute, Kermanshah, University of Medical Sciences, Kermanshah, Iran.
Department of Molecular Medicine, School of Medicine, Kermanshah, University of Medical Sciences, Kermanshah, Iran.
Inflamm Res. 2021 Jul;70(7):749-752. doi: 10.1007/s00011-021-01469-8. Epub 2021 Jun 26.
Coronavirus disease 2019 (COVID-19) pandemic is still a world-class challenge. Inflammation, especially its severe form with excess release of pro-inflammatory cytokines (cytokine storm) which is a life-threatening condition, is among the most important suspects involved in COVID-19 pathogenesis. It has been shown that cytokine storm could cause notable morbidities such as acute respiratory distress syndrome (ARDS) which leads to hypoxia which is significantly associated with mortality of patients with COVID-19. Hypoxia-inducible factor 1α (HIF-1α) which activates following ARDS-induced hypoxia plays a crucial role in pathogenesis of cytokine storm. The expression of tumor necrosis factor α (TNF-α), interleukin 1 β (IL-1β), and IL-6 which are key elements of cytokine storm are by nuclear factor κβ (NFκB). Interestingly, during the hypoxia, HIF-1α activates NFκB to induce expression of pro-angiogenic and pro-inflammatory factors. These released factors starts a autocrine/paracrine loop and causes deterioration of their etiological pathways of expression: cytokine storm and ARDS. To sum up, it seems HIF-1α is an important target to hit to ameliorate the mentioned pathways. Herein, we suggest perfluorocarbons (PFCs) which are among the organofluorine compounds as a possible co-treatment to reduce hypoxemia and then hypoxia. These substances are known for their high gas solving potential that make them able to be used as a synthetic artificial blood product. Due to the potential of PFCs to affect the fountain of important physiopathological pathway such as inflammation a hypoxia through affecting NFκB, they could be considered as multi-target co-treatment for ARD individuals with COVID-19. It is highly suggested to evaluate this hypothesis in following researches.
新型冠状病毒病(COVID-19)大流行仍然是一个世界级的挑战。炎症,尤其是其严重形式伴有促炎细胞因子(细胞因子风暴)的过度释放,这是COVID-19发病机制中的最重要的可疑因素之一。已经表明,细胞因子风暴可导致明显的发病率,例如急性呼吸窘迫综合征(ARDS),这会导致缺氧,这与 COVID-19 患者的死亡率显著相关。低氧诱导因子 1α(HIF-1α)在 ARDS 诱导的缺氧后被激活,在细胞因子风暴发病机制中起着关键作用。细胞因子风暴的关键要素肿瘤坏死因子α(TNF-α)、白细胞介素 1β(IL-1β)和白细胞介素 6(IL-6)的表达受核因子κB(NFκB)调控。有趣的是,在缺氧期间,HIF-1α激活 NFκB 诱导促血管生成和促炎因子的表达。这些释放的因子启动自分泌/旁分泌循环,导致其表达的病因途径的恶化:细胞因子风暴和 ARDS。总之,似乎 HIF-1α是改善这些途径的重要靶点。在此,我们建议使用全氟化碳(PFC)作为可能的联合治疗方法来减轻低氧血症,然后是缺氧。这些物质因其高气体溶解度而闻名,这使它们能够用作合成人工血液产品。由于 PFC 可能通过影响 NFκB 影响炎症和缺氧等重要生理病理途径的源头,因此它们可被视为 COVID-19 合并 ARD 患者的多靶点联合治疗方法。强烈建议在后续研究中评估这一假设。